Loss of renal function and microvascular blood flow after suprarenal aortic clamping and reperfusion (SPACR) above the superior mesenteric artery is greatly augmented compared with SPACR above the renal arteries.
Loss of renal function and microvascular blood flow after suprarenal aortic clamping and reperfusion (SPACR) above the superior mesenteric artery is greatly augmented compared with SPACR above the renal arteries.
复制标题
与肾动脉上方的 SPACR 相比，肠系膜上动脉上方的肾上主动脉阻断和再灌注 (SPACR) 后肾功能和微血管血流的丧失大大增加。
DOI：
10.1016/j.jvs.2006.10.045
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发表时间：
2007
影响因子：
4.3
通讯作者：
Myers,DanielJ
中科院分区：
文献类型：
--
作者：
Myers,StuartI;Wang,Li;Myers,DanielJ
目的肾功能不全仍然是影响肾上动脉瘤和肾动脉闭塞症治疗后患者的并发症。据我们所知，目前尚无资料显示肾动脉上方的肾上主动脉阻断再灌注(SRACR)与肠系膜上动脉上方的SRACR(SMA-SRACR)相比可保护肾功能。本研究验证了SMA-SRACR引起的肾血流和功能的下调比肾-SRACR更严重的假说，这是由于全身氧自由基(ODFR)释放的增加。方法麻醉SD大鼠(约350g)，将微透析探头或激光多普勒纤维插入肾皮质(深度2 mm)和肾髓质(深度4 mm)。连续监测激光多普勒血流，将微透析探头连接到注射器泵上，以3μ/m in的速度向体内灌流乳酸林格液。SMA-SRACR下调皮质诱导型一氧化氮合酶，而肾-SRACR不下调。皮质和髓质对血流减少和NO合成的反应是前列腺素E_2合成增加，这是由于环氧合酶-2含量增加所致。超氧化物歧化酶可恢复SMA-SRACR(但不能恢复肾-SRACR)皮质和髓质的NO合成，提示肠系膜缺血再灌注时产生的ODFR是SMA-SRACR模型肾脏NO合成减少的系统机制之一。SMA-SRACR术后内生肌酐清除率下降90%，降幅大于肾SMA-SRACR后的60%。结论SMA-SRACR和SMA-SRACR后，NO在维持肾皮质和髓质血流及NO合成中起重要作用。这些结果还表明，除上述两种模型所致的肾缺血再灌流外，SMA SRACR还可诱导肠系膜缺血再灌流，导致ODFR的产生，从而导致肾皮质和髓质NO合成减少。维持内脏血流量或试图将SRACR保持在SMA水平以下可能有助于制定策略，将SRACR后的肾脏损伤降至最低。
OBJECTIVERenal insufficiency continues to be a complication that can affect patients after treatment for suprarenal aneurysms and renal artery occlusive disease. To our knowledge, no data are available showing that suprarenal aortic clamping and reperfusion (SRACR) above the renal arteries (renal-SRACR) preserves renal function compared with SRACR above the superior mesenteric artery (SMA-SRACR). This study examined the hypothesis that SMA-SRACR–induced downregulation of renal blood flow and function is more severe than renal-SRACR owing to the addition of systemic oxygen-derived free radical (ODFR) release.METHODSMale Sprague-Dawley rats (about 350 g) were anesthetized and microdialysis probes or laser Doppler fibers were inserted into the renal cortex (depth of 2 mm) and into the renal medulla (depth of 4 mm). Laser Doppler blood flow was continuously monitored, and the microdialysis probes were connected to a syringe pump and perfused in vivo at 3 μL/min with lactated Ringer’s solution.RESULTSSMA-SRACR and Renal-SRACR decreased medullary and cortical blood flow and nitric oxide (NO) synthesis. SMA-SRACR downregulated cortical inducible NO synthase, whereas renal-SRACR did not. The cortex and medulla responded to the decreased blood flow and NO synthesis by increasing in prostaglandin E2synthesis, which was due to increased cyclooxygenase-2 content. Superoxide dismutase restored SMA-SRACR (but not renal-SRACR) cortical and medullary NO synthesis, suggesting that ODFRs generated during mesenteric ischemia–reperfusion were one of the systemic mechanisms contributing to decreased renal NO synthesis in the SMA-SRACR model. The 90% decrease in creatinine clearance after SMA-SRACR was greater than the 60% decrease after renal-SRACR.CONCLUSIONSThese data show that NO is important in maintaining renal cortical and medullary blood flow and NO synthesis after renal and SMA-SRACR. These data also suggest that in addition to the renal ischemia–reperfusion caused by both models, SMA SRACR induces mesenteric ischemia–reperfusion, resulting in the generation of ODFRs, which contribute to decreased renal cortical and medullary NO synthesis. Maintaining splanchnic blood flow or attempting to keep SRACR below the SMA level may be helpful in developing strategies to minimize the renal injury after SRACR.